Detecção molecular de Neospora caninum em macaco-da-noite (Aotus azarae) de vida livre no estado do Mato Grosso: relato de caso / Molecular detection of Neospora caninum in azara's night monkey (Aotus azarae) of wildlife in the state of Mato Grosso: Case report

Estudos indicam, por meio de infecção experimental, que primatas não humanos são susceptíveis à infecção por Neospora caninum. Relata-se um caso de um macaco-da-noite (Aotus azarae infulatus), que apresentou sinais inespecíficos e não respondeu à terapêutica clínica de suporte, evoluindo a óbito, encaminhado em seguida para exame anatomopatológico. Amostras de tecidos foram coletadas e processadas rotineiramente para confecção de lâminas histológicas. Microscopicamente, a principal lesão foi observada no coração e consistia em miocardite necrótica multifocal por protozoário, com a presença de estruturas compatíveis com o estágio de taquizoítos de protozoários dos gêneros Neospora sp. ou Toxoplasma sp. No sistema nervoso central, predominantemente no tronco encefálico, havia estruturas semelhantes às descritas no coração. Os resultados da reação em cadeia pela polimerase (PCR) foram positivos para N. caninum e negativos para Toxoplasma gondii, usando DNA extraído do sangue e dos tecidos. Este relato de caso fornece evidências histológicas e moleculares de que o primata em questão foi susceptível a uma infecção natural, porém estudos devem ser realizados para investigar o real papel dos primatas no ciclo de vida de N. caninum.(AU)

Studies indicate through experimental infection that non-human primates are susceptible to infection by Neospora caninum. This report is of a case of a night monkey (Aotus azarae infulatus) that presented nonspecific signs and did not respond to supportive clinical therapy evolving to death, followed by a pathology examination. Tissue specimens were routinely collected and processed for the preparation of histological slides. Microscopically, the main lesion was observed in the heart and consisted of multifocal necrotic myocarditis by protozoa, with the presence of structures compatible with the stage of protozoan tachyzoites of the genus Neospora sp. or Toxoplasma sp. In the central nervous system, predominantly in the brainstem there were structures similar to those described in the heart. Polymerase chain reaction (PCR) results were positive for N. caninum and was negative for Toxoplasma gondii using DNA extracted from blood and tissues. This case report provides histological and molecular evidence that the primate in question was susceptible to a natural infection, but studies should be conducted to investigate the real role of primates in the life cycle of N. caninum.(AU)

Effect of 0, 15% sodium hialuronate and 0, 5% carboxymethylcellulose on tear film breakup time in healthy dogs and in dogs with keratoconjunctivitis sicca / Efeito do hialuronato de sódio a 0, 15% e da carboximetilcelulose sódica a 0, 5% no tempo de ruptura do filme lacrimal de cães saudáveis e com ceratoconjuntivite seca

This study aimed to evaluate the effect of the 0.15% sodium hyaluronate (SH) and of 0.5% carboxymethylcellulose (CMC) on tear film breakup time (TFBUT) in 10 healthy dogs and in 32 eyes of dogs with keratoconjunctivis sicca (KCS). In addition, the goblet cell density (GCD) of this population was quantified. TFBUT was assessed at baseline and at different time points following the instillation of SH and CMC. KCS was graded as mild, moderate, and severe. GCD were quantified from conjunctival biopsies. The number of GCD differed significantly between patients with mild and moderate KCS (P<0.01). TFBUT of healthy dogs increased only for 1 minute after treatment with SH (P<0.01). Regarding baseline and treatments, SH significantly increased TFBUT for up to 30 minutes on the ocular surface, in comparison to CMC, in all categories of KCS (P<0.01). TFBUT and GCD correlated positively when the healthy and diseased eyes were grouped (r=0.41, P=0.006). It can be concluded that in dogs with KCS, SH lasts longer periods on the ocular surface than CMC, but such agents does not increase TFBUT in healthy dogs. Additionally, tear film stability tends to reduce in a linear fashion from the mild to severe form of KCS.(AU)

Objetivou-se avaliar os efeitos do hialuronato de sódio a 0,15% (HS) e da carboximetilcelulose a 0,5% (CMC) no teste de ruptura do filme lacrimal (TRFL) em 10 cães saudáveis e em 32 olhos de cães com ceratoconjuntivite seca (CCS). Ademais, quantificou-se a densidade de células caliciformes (DCC) deles. Mensurou-se o TRFL em momentos distintos antes e após a instilação do HS e da CMC. Graduou-se a CCS em leve, moderada e severa. Quantificou-se a DCC a partir de biópsias conjuntivais. A DCC diferiu apenas entre pacientes com CCS leve e severa (P<0,01). Em cães saudáveis, o TRFL se elevou apenas após um minuto do tratamento com HS (P<0,01). Relativamente ao período basal e entre os tratamentos, o HS elevou o TRFL de forma mais eficaz e permaneceu por até 30 minutos na superfície ocular, comparativamente à CMC, em todas as categorias de CCS (P<0,01). Ao se agruparem os olhos saudáveis e os com CCS, o TRFL se correlacionou com a DCC (r=0.41, P=0.006). Conclui-se que o HS permanece por maior tempo na superfície ocular que a CMC em cães com CCS, mas que tais substâncias não elevam o TRFL em cães saudáveis. Ademais, a estabilidade do filme lacrimal tende a se reduzir de modo linear da forma leve até à severa da CCS.(AU)

Effect of intracerebroventricularly injected insulin on urinary sodium excretion by cerebroventricular streptozotocin-treated rats

Recent evidence suggests that insulin may influence many brain functions. It is known that intracerebroventricular (icv) injection of nondiabetogenic doses of streptozotocin (STZ) can damage insulin receptor signal transduction. In the present study, we examined the functional damage to the brain insulin receptors on central mechanisms regulating glomerular filtration rate and urinary sodium excretion, over four periods of 30 min, in response to 3 æl insulin or 0.15 NaCl (vehicle) injected icv in STZ-treated freely moving Wistar-Hannover rats (250-300 g). The icv cannula site was visually confirmed by 2 percent Evans blue infusion. Centrally administered insulin (42.0 ng/æl) increased the urinary output of sodium (from 855.6 ± 85.1 to 2055 ± 310.6 delta percent/min; N = 11) and potassium (from 460.4 ± 100 to 669 ± 60.8 delta percent/min; N = 11). The urinary sodium excretion response to icv insulin microinjection was markedly attenuated by previous central STZ (100 æg/3 æl) administration (from 628 ± 45.8 to 617 ± 87.6 delta percent/min; N = 5) or by icv injection of a dopamine antagonist, haloperidol (4 æg/3 æl) (from 498 ± 39.4 to 517 ± 73.2 delta percent/min; N = 5). Additionally, insulin-induced natriuresis occurred by increased post-proximal tubule sodium rejection, despite an unchanged glomerular filtration rate. Excluding the possibility of a direct action of STZ on central insulin receptor-carrying neurons, the current data suggest that the insulin-sensitive response may be processed through dopaminergic D1 receptors containing neuronal pathways

Fighting by sleep-deprived rats as a possible manifestation of panic: effects of sodium lactate

Increased fighting is an effect of desynchronized sleep deprivation (DSD) in rats, and recently this behavior has been suggested to be spontaneous panic and equivalent to panic disorder. In the present study we tested this hypothesis by evaluating the effect of sodium lactate on this aggressiveness, because this substance is recognized to induce spontaneous panic attacks in patients. A total of 186 male albino Wistar rats, 250-350 g, 90-120 days of age, were submitted to DSD (multiple platform method) for 0, 4, or 5 days. At the end of the deprivation period the rats were divided into subgroups respectively injected intraperitoneally with 1.86, 2.98 and 3.72 g/kg of 1 M sodium lactate, or 1.86 and 3.72 g/kg of 2 M sodium lactate. The control animals were submitted to the same procedures but received equivalent injections of sodium chloride. Regardless of DSD time, sleep-deprived animals that received sodium lactate presented a significantly higher mean number of fights (0.13 + or - 0.02 fights/min) and a longer mean time spent in confrontation (2.43 + or - 0.66 s/min) than the controls (0.01 + or - 0.006 fights/min and 0.12 + or - 0.07 s/min, respectively; P<0.01, Student t-test). For the sodium lactate group, concentration of the solution and time of deprivation increased the number of fights, with the mean number of fights and mean duration of fighting episodes being greater with the 2.98 g/kg dose using 1 M lactate concentration. These results support the hypothesis that fighting induced by DSD is probably a spontaneous panic manifestation. However, additional investigations are necessary in order to accept this as a promising animal model for studies on panic disorder